Timothy E. O'Connor

Structure of a murine leukemia virus after disruption with tween-ether and comparison with two myxoviruses

Abstract The effects of treatment with Tween-ether (TE) on physical and morphological properties of Rauscher leukemia virus (RLV) were studied and compared with those obtained on two myxoviruses (NDV and PR8 influenza virus). TE treatment readily produced viral disruption. The buoyant density of the released internal components was similar in all three cases, and greater than that of the intact virus. Electron microscopic study of intact and TE-treated virus was performed. (1) NDV easily released its characteristic nucleocapsid. PR8 influenza virus was more resistant to disruption and the internal component appeared as a coiled cylinder 70 A in diameter. (2) Preparations of intact Rauscher virus showed two types of virions: the “immature” type where two concentric shells were enclosed in the viral envelope, and the “mature” virion where a dense nucleoid was enclosed in the envelope. (3) Treatment with Tween-ether readily removed the envelope of RLV, as seen in thin sections of TE-treated preparations. (4) Ringlike profiles appeared in negatively stained preparations of the aqueous phase of RLV. These ring profiles were 750–850 A in diameter, 75 A thick, with two threads and a central circular core, 15–25 A in diameter. Morphological units and possible helical structure appeared in these structures which corresponded in size to the outer shell of the immature virions. (5) Dense, spherical bodies, 700–750 A in diameter, were also present in the aqueous phase. They represented the naked dense nucleoids of the mature virions. (6) Ribonuclease treatment performed on TE-treated RLV resulted in a significant decrease of the stainability of the naked nucleoids, the same treatment was ineffective on virus not treated by TE. (7) The structure of RLV has been envisioned and compared with that of other types of virus. The outer shell of the immature virion may represent the capsid of the virus, made up of a coiled cylinder. The genetic material appears to lie more internally in the inner shell. The structure of the mature virion results from the collapse of the two shells inside the envelope.

Viral Infection Across Species Barriers: Reversible Alteration of Murine Sarcoma Virus for Growth in Cat Cells

Infection of cat embryo cells by a centrifugally induced aggregate of murine sarcoma virus and feline leukemia virus gave rise to a defective, focus-forming virus which propagated in cat cells, but not in mouse cells. This virus, apparently enveloped with a feline leukemia virus coat, was later subjected to aggregation with murine leukemia virus, whereupon it regained the capacity for growth in mouse cells.

Titration Patterns of a Murine Sarcoma-Leukemia Virus Complex: Evidence for Existence of Competent Sarcoma Virions

Stocks of inurine sarcoma virus show titration patterns ranging from one-to two-hit kinetics. The comparison of various titrations of this virus, both with and without added helper virus, to theoretical model systems composed of defined constituents, suggests the existence of a sarcoma virus that does not need coinfectinig murine leukemia virus to be manifested as a focus-forming unit. The behavior of such nondefective particles is compatible with a postulated leukemia-sarcoma virus hybrid.

Replication of defective and competent forms of murine sarcoma virus in mouse cell cultures

Abstract The propagation of each of the known constituents of murine sarcoma virus stocks—competent MSV, defective MSV, and endogenous MuLV—was studied in three different mouse cell culture systems: Swiss mouse embryo, the established 3T3 cell line, and neonatal Swiss mouse kidney secondary cultures. All the viral components of the MSV complex adsorbed to the same degree to all three cell types. MuLV alone grew well in the embryo culture, grew poorly in the 3T3 cell line and very poorly in the kidney cultures. A defective MSV-MuLV mixture propagated rapidly in the embryo cultures and eventually yielded some competent MSV progeny. Propagation of the defective MSV-MuLV mixture was poor in the 3T3 cell line and and barely detectable in the kidney cultures. In the 3T3 cell, the slow rate of defective MSV growth was not enhanced by the addition of exogenous MuLV. In contrast, virus stocks consisting predominantly of competent MSV propagated rapidly and well in all three cell systems. In embryo cells competent MSV gave rise to virus progeny composed of a mixture of defective and competent MSV. Infection of 3T3 cells with competent virus resulted in initially defective, and later in some competent, MSV. In mouse kidney cells the progeny of competent MSV consisted of predominantly defective MSV, a small amount of competent virus, and very little MuLV. These findings define the superior infective capacity of competent MSV and the modulation of the composition of the sarcoma-leukemia virus complex during propagation in various mouse cell systems.

Radiation Leukemia Virus: Quantitative Tissue Culture Assay

Radiation leukemia virus does not propagate in tissue cultures from either Swiss or C57BL mouse embryos, but it does augment focus formation by the defective Moloney leukemia pseudotype of murine sarcoma virus in Swiss mouse cells and thus can be quantitatively assayed.

Murine Leukemia Viruses: Antigenic Studies by Quantitative Complement Fixation

The murine leukemia viruses of Rauscher and Friend, derived from plasnma of infected Balb/c mice, was purified. Their antigenic relationship was studied by quantitative complement-fixation reactions with the virion antigen and homologous antiserums. The complement-fixation curves observed in cross-reactions indicated close antigenic similarity between these two leukemia viruses. Highly purified viral preparations contained detectable amounts of host antigens.